Basic Study
Copyright ©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 21, 2021; 27(3): 240-254
Published online Jan 21, 2021. doi: 10.3748/wjg.v27.i3.240
Circular RNA AKT3 governs malignant behaviors of esophageal cancer cells by sponging miR-17-5p
Hong-Liang Zang, Fu-Jian Ji, Hai-Ying Ju, Xiao-Feng Tian
Hong-Liang Zang, Xiao-Feng Tian, Department of Hepatobiliary and Pancreatic Surgery, China-Japan Union Hospital of Jilin University, Changchun 130033, Jilin Province, China
Fu-Jian Ji, Department of Colorectal Surgery, China-Japan Union Hospital of Jilin University, Changchun 130033, Jilin Province, China
Hai-Ying Ju, Department of Hematology, Jilin Province Blood Center, Changchun 130000, Jilin Province, China
Author contributions: Zang HL contributed to the study design and reviewed the manuscript; Ji FJ and Tian XF analyzed the data and wrote the manuscript; Ju HY and Zang HL contributed to the data collection, data interpretation, and manuscript writing; all authors read and approved the final manuscript.
Institutional review board statement: This research was reviewed and approved by the Ethics Committee of China-Japan Union Hospital of Jilin University and complied with the guidelines of Declaration of Helsinki.
Institutional animal care and use committee statement: The procedures were in accordance with guidelines of Animal Use and Care Committee of China-Japan Union Hospital of Jilin University.
Conflict-of-interest statement: All the authors have no conflict of interest related to the manuscript.
Data sharing statement: No additional data are available.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Xiao-Feng Tian, MD, Chief Doctor, Department of Hepatobiliary and Pancreatic Surgery, China-Japan Union Hospital of Jilin University, No. 126 Xiantai Street, Erdao District, Changchun 130033, Jilin Province, China. fengwykctut4210@163.com
Received: October 30, 2020
Peer-review started: October 30, 2020
First decision: November 30, 2020
Revised: December 4, 2020
Accepted: December 16, 2020
Article in press: December 16, 2020
Published online: January 21, 2021
Processing time: 76 Days and 5.2 Hours
ARTICLE HIGHLIGHTS
Research background

Esophageal cancer is one of the most malignant tumors in the digestive system and exploring the underlying mechanism is a key issue that needs to be addressed. Circular RNA AKT3 (circAKT3) is a novel noncoding RNA participating in the development and progression of multiple tumors.

Research motivation

To identify biomarkers for the diagnosis and treatment of esophageal cancer.

Research objectives

To explore the mechanism of the role of circAKT3 in the development of esophageal cancer.

Research methods

Cell Counting Kit-8, wound healing assay, Transwell assay, and fluorescence analysis were used to evaluate the circAKT3 effect on proliferation, migration, invasion, and apoptosis of esophageal cancer cells.

Research results

In vitro assays results revealed that proliferative, migratory, and invasive capacities of esophageal cancer cells were significantly enhanced by circAKT3 overexpression. miR-17-5p was screened as the target of circAKT3, and miR-17-5p antagonized the effects of circAKT3 on esophageal cancer cells. Moreover, we identified RHOC and STAT3 as the direct target molecules of miR-17-5p, and circAKT3 facilitated expression of RHOC and STAT3 by inhibiting miR-17-5p. In vivo assays showed circAKT3 knockdown inhibited growth of esophageal cancer.

Research conclusions

CircAKT3 enhanced proliferative, migratory, and invasive capacities of esophageal cancer cells by sponging miR-17-5p to exert protumor effects, and downregulation of circAKT3 inhibited xenograft tumor growth of esophageal cancer in vivo, providing a potential target for better understanding the underlying mechanism of esophageal cancer.

Research perspectives

The role of circAKT3 in other tumors may be uncovered in the future, and its application in anticancer therapy will be promoted.